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Results for “MONILIASIS, CUTANEOUS”

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At least 145 records · Page 8Linked to original sources
PubMed1976

Hypersensitivity as a cause of dermatologic and vaginal moniliasis resistant to topical therapy.

The finding of multiple respiratory or skin allergies together with a high rate of improvement by desensitization leads the author to conclude that allergy is a predisposing factor for the chronicity or recurrence of vaginal or dermatologic moniliasis. Desensitization with Candida albicans antigen was the mainstay in the treatment of resistant dermatologic or vaginal moniliasis and the sole form of therapy in cases of nail involvement with deep seated lesions out of the reach of topical agents.

Candidiasis, Cutaneous↗
PubMed1978

The role of microorganisms in diaper dermatitis.

A quantitative microbiological survey of multiple sites in the diaper area in 40 normal infants and 100 infants with various forms of diaper dermatitis showed (1) no significant differences between normal infants and those with common chafing form of diaper dermatitis except for a low number of Staphylococcus aureus organisms in 50% of those with chafing dermatitis compared to no S aureus in normals; (2) S aureus occurred in high numbers in every case of atopic dermatitis and was frequently found at much lower levels in psoriasis, seborrheic dermatitis, and chafing dermatitis; (3) Candida albicans occurred in 80% of cases clinically diagnosed as moniliasis localized to the diaper area and in 33% of those suspected of Candida infection with dissemination beyond the diaper area, while C albicans was found in only five of 145 culture sites in 40 normal infants.

Candida albicans↗
PubMed1978

[The occurrence of nappy rash at a children's hospital and its treatment with Canesten (author's transl)].

An unselected, mycologically-controlled trial was conducted at the University Children's Hospital of Graz on the treatment of nappy rash by the topical application of Canesten (clotrimazole), a broad-spectrum mycotic in the form of a 1% cream. 56 children, ranging in age from 3 weeks to 41/2 years, were treated for thrush, principally located in the genital area. Only some of the children were admitted primarily on account of the oral and/or perianal moniliasis. The majority of the children were hospitalized for some other reason and thrush was diagnosed as an accompanying condition. Candida albicans proved to be the most frequent pathogenic organism. The results of therapy were judged according to mycological and clinical criteria. The mycological findings became negative in 54 out of the 56 children. Clinical improvement was apparent in all cases between the 5th and 10th day of therapy; complete recovery occurred between the 5th and 25th day, depending on the extent and localization of the moniliasis. One child showed improvement in, but not recovery from the disease, because therapy was interrupted on premature discharge from hospital. Therapy was unsuccessful in the remaining child, although slight improvement occurred. Tolerance was good in all patients on application of Canesten cream thrice daily.

Administration, Topical↗
PubMed1986

Inherited susceptibility to autoimmune Addison's disease is linked to human leukocyte antigens-DR3 and/or DR4, except when associated with type I autoimmune polyglandular syndrome.

The inherited susceptibility to autoimmune Addison's disease was found to be strongly associated with human leukocyte antigens (HLA)-DR3 and DR4 alleles. In a study of 45 white patients from the United States with the disease, the relative risks (the number of times that an individual is at risk for Addison's disease if they had a marker, compared to those without such marker) were found to be 6.0, 4.6, and 26.5 for the DR3 allele, the DR4 allele, and for DR3/DR4 heterozygotes, respectively. Frequencies of DR2, DR5, and DR7 in the patients with Addison's disease were significantly decreased in comparison to 265 individuals in the control population. These HLA-DR frequencies in patients with Addison's disease were similar to those for 723 patients with insulin-dependent diabetes (IDD). However, the above HLA-DR associations persisted even when only data from the 37 patients with Addison's disease who did not have IDD were considered. Adrenocortical autoantibodies in 23 patients with IDD who did not have Addison's disease were equally frequent among those with DR4 and DR3 alleles. In contrast, HLA-DR frequencies in 17 patients with type I autoimmune polyglandular syndrome (chronic mucocutaneous moniliasis, hypoparathyroidism, Addison's disease, etc.) were not different from control. We conclude that genetic susceptibility to autoimmune Addison's disease may involve the same HLA-associated genetic determinants as IDD, except when Addison's disease occurs as part of type I autoimmune polyglandular syndrome.

Addison Disease↗